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Coming of Age: CD96 Emerges as Modulator of Immune Responses
Hristo Georgiev1, Inga Ravens1, Georgia Papadogianni1
1Institute of Immunology, Hannover Medical School, Hannover, Germany.
Insights
CD96 protein inhibits natural killer (NK) cells, impacting tumor containment. Blocking CD96 shows therapeutic potential against cancer metastasis.
Area of Science:
- Immunology
- Molecular Biology
- Cancer Research
Background:
- CD96 (cluster of differentiation 96) is an immunoglobulin superfamily member expressed on T and NK cells.
- CD96 interacts with CD155 on target cells, inhibiting mouse NK cell activity.
- Previous studies suggest blocking CD96 enhances anti-tumor effects in murine models.
Purpose of the Study:
- To review the structural features and functions of CD96.
- To explore unresolved aspects of CD96, including species-specific activation differences.
- To discuss CD96's role within the CD155, CD96, CD226, and TIGIT immune regulatory network.
Main Methods:
- Literature review of structural and functional studies on CD96.
- Analysis of CD96 interactions with its ligand CD155.
- Comparative analysis of CD96 function in mouse and human systems.
Main Results:
- CD96's interaction with CD155 inhibits NK cell activity, affecting tumor metastasis.
- Absence of CD96-CD155 interaction demonstrates anti-metastatic effects in mouse models.
- Potential species-specific activation differences between human and mouse CD96 warrant further investigation.
Conclusions:
- Understanding CD96 structure-function relationships is crucial for cancer therapy development.
- CD96's role in immune regulation, particularly within the CD155/CD96/CD226/TIGIT axis, requires further elucidation.
- Targeting CD96 presents a promising strategy for enhancing anti-tumor immunity and treating cancer metastasis.
Abstract:
CD96 represents a type I transmembrane glycoprotein belonging to the immunoglobulin superfamily. CD96 is expressed mainly by cells of hematopoietic origin, in particular on T and NK cells. Upon interaction with CD155 present on target cells, CD96 was found to inhibit mouse NK cells, and absence of this interaction either by blocking with antibody or knockout of CD96 showed profound beneficial effects in containment of tumors and metastatic spread in murine model systems. However, our knowledge regarding CD96 functions remains fragmentary. In this review, we will discuss structural features of CD96 and their putative impact on function as well as some unresolved issues such as a potential activation that may be conferred by human but not mouse CD96. This is of importance for translation into human cancer therapy. We will also address CD96 activities in the context of the immune regulatory network that consists of CD155, CD96, CD226, and TIGIT.
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